Evidence map›Paper›PMID 30639098›Full record

ArticleCell2019

Genome-wide CRISPR Screens in T Helper Cells Reveal Pervasive Crosstalk between Activation and Differentiation.

Johan Henriksson, Xi Chen, Tomás Gomes, Ubaid Ullah, Kerstin B Meyer, Ricardo Miragaia, Graham Duddy, Jhuma Pramanik, Kosuke Yusa, Riitta Lahesmaa and 1 more

Abstract read
In one paragraph

Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

137 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. ANKRD11 deficiency reprograms CD8Nature immunology · 2026
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  10. The phospholipid profile of T cells shapes ACSL4 dependency and ferroptosis sensitivity of naive, effector, and memory T cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
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77 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Johan HenrikssonWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK; Department of Biosciences and Nutrition, Karolinska Institutet, Hälsovägen 7, Novum, SE-141 83, Huddinge, Sweden.
Xi ChenWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Tomás GomesWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Ubaid UllahTurku Centre for Biotechnology, University of Turku and Åbo Akademi University, Tykistökatu 6 FI-20520, Turku, Finland.
Kerstin B MeyerWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Ricardo MiragaiaWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Graham DuddyWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Jhuma PramanikWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Kosuke YusaWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Riitta LahesmaaTurku Centre for Biotechnology, University of Turku and Åbo Akademi University, Tykistökatu 6 FI-20520, Turku, Finland.
Sarah A TeichmannWellcome Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK; EMBL-European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SD, UK; Theory of Condensed Matter, Cavendish Laboratory, 19 JJ Thomson Ave, Cambridge CB3 0HE, UK. Electronic address: st9@sanger.ac.uk.

Funding

Wellcome TrustWellcome Trust WT206194
6 · The paper itself

Abstract

T helper type 2 (Th2) cells are important regulators of mammalian adaptive immunity and have relevance for infection, autoimmunity, and tumor immunology. Using a newly developed, genome-wide retroviral CRISPR knockout (KO) library, combined with RNA-seq, ATAC-seq, and ChIP-seq, we have dissected the regulatory circuitry governing activation and differentiation of these cells. Our experiments distinguish cell activation versus differentiation in a quantitative framework. We demonstrate that these two processes are tightly coupled and are jointly controlled by many transcription factors, metabolic genes, and cytokine/receptor pairs. There are only a small number of genes regulating differentiation without any role in activation. By combining biochemical and genetic data, we provide an atlas for Th2 differentiation, validating known regulators and identifying factors, such as Pparg and Bhlhe40, as part of the core regulatory network governing Th2 helper cell fates.

Indexed as

AnimalsCell DifferentiationChromatinClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsGenomeHigh-Throughput Nucleotide SequencingHumansLymphocyte ActivationMiceMice, Inbred C57BLReceptor Cross-TalkTh2 CellsT-Lymphocytes, Helper-InducerTranscription FactorsChromatinTranscription FactorsATAC-seqCas9CD4 T helper cellChIP-seqCRISPRknockoutmouseoverexpressionpooled screenretrovirus

Identifiers

PMID30639098
PMCPMC6370901

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.